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Year : 2013  |  Volume : 16  |  Issue : 4  |  Page : 171-173

Acute flaccid quadriparesis and distal symmetrical polyneuropathy complicating tuberculosis of the urinary tract

1 Department of Medicine, Ahmadu Bello University Teaching Hospital, Shika, Zaria, Nigeria
2 Department of Medicine, Niger Delta University, Ammasoma, Bayelsa, Nigeria
3 Department of Radiology, Ahmadu Bello University Teaching Hospital, Shika, Zaria, Nigeria

Date of Web Publication21-Jan-2014

Correspondence Address:
Onyeadumarakwe R Obiako
Department of Medicine, Ahmadu Bello University Teaching Hospital, Shika, Zaria
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DOI: 10.4103/1118-8561.125575

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Acute flaccid quadriparesis and distal symmetrical polyneuropathy (DSP) are neurological conditions associated with sudden compression of the cervical spinal cord and damage to peripheral nerves, respectively. Although quadriparesis can result from compressive myelopathy by tuberculosis (TB) of the cervical spine, it has not been reported in patients with TB of the urinary tract, either alone or in combination with DSP. We therefore report the case of a 28-year-old man who developed sudden weakness of the four limbs after 2 months of low grade fever, night sweats, malaise, and weight loss; followed by 2 weeks of low back pain, tingling sensations, and numbness of both hands and feet; all without evidence of compressive myelopathy. A diagnosis of TB of the urinary tract was made following positive Mantoux test and isolation of acid fast bacilli from one of six urine samples, and patient underwent 12 months course of antituberculous therapy with resolution of symptoms and signs of both TB infection and neurological diseass. This report has shown that anti TB therapy is effective in both TB of the urinary tract and the associated neurological complications. This report demonstrates a rare neurological complication of urinary tract Tb and the efficacy of anti TB therapy in both conditions

Keywords: Acute flaccid quadriparesis, polyneuropathy, tuberculosis, urinary tract

How to cite this article:
Obiako OR, Ogoina D, Kehinde JA, Iheonye H, Nkoro TK, Hamidu AU. Acute flaccid quadriparesis and distal symmetrical polyneuropathy complicating tuberculosis of the urinary tract. Sahel Med J 2013;16:171-3

How to cite this URL:
Obiako OR, Ogoina D, Kehinde JA, Iheonye H, Nkoro TK, Hamidu AU. Acute flaccid quadriparesis and distal symmetrical polyneuropathy complicating tuberculosis of the urinary tract. Sahel Med J [serial online] 2013 [cited 2022 Jan 22];16:171-3. Available from: https://www.smjonline.org/text.asp?2013/16/4/171/125575

  Introduction Top

Tuberculosis (TB) is a disease with varied and protean manifestations, most of which are pulmonary or extrapulmonary. Extrapulmonary TB is responsible for most of the systemic complications of TB. For instance, in patients with compression of the spinal cord by TB of the cervical spine, spastic quadriparesis is the usual presentation but during the acute phase of neuronal shock, affected individuals may present with flaccid quadriparesis. [1]

TB of the genitourinary tract accounts for about 15% of all extrapulmonary TB infections and may involve any portion of the tract. It is usually due to hematogenous seeding following primary infection, and can be recognized if there are local symptoms of urinary frequency, dysuria, hematuria, and flank pain; or those of involvement of genital organs such as infertility, pelvic pain, and menstrual abnormalities (in females), epididymo-orchitis and prostatitis (in males). [2]

The urine is acidic and yields pus and red cells on microscopy. In 90% of cases, urine is culture-negative; [2] thus, the disease can be misdiagnosed or missed in a patient who has no local symptoms and signs. However, the infection has a good prognosis as it responds well to antituberculous therapy. [3]

Although acute flaccid quadriparesis and distal symmetrical polyneuropathy (DSP) have been described in many medical conditions, they have not been described in patients with TB of the urinary tract.

  Case Report Top

BM, a 28 year old bachelor presented with 2 months history of low grade fever, night sweats, malaise and weight loss; 2 weeks of low back pain, feet dysesthesia and quadriparesis in a distal to proximal fashion. He had no visual, respiratory, cardiovascular, abdominal, and genitourinary symptoms. He had no notable pre-morbid medical or surgical history; no contact with a TB patient, farm animals or animal products; and had not been exposed to sexual intercourse or blood transfusion. He neither ingested alcohol nor smoked cigarettes.

On examination, he was ill-looking and mildly febrile (T = 37.4°C), not pale, no significant peripheral lymphadenopathy and no pedal edema. His pulse rate was 92 beats/min and regular with a normal blood pressure of 120/70 mmHg. Heart sounds were normal. Chest and abdominal examinations were normal. He was fully conscious and alert with normal mentation, and cranial nerves functions. There were no signs of meningeal irritation or muscle wasting, but there were generalized hypotonia and hyporeflexia. Muscle power in upper and lower limbs were 3/5 and 0/5 respectively. There was a loss of proprioception in a glove and stocking distribution, but no definite sensory level, saddle anesthesia or incontinence. The vertebral spine was normal and non-tender.

Tuberculin skin (Mantoux) test was 20 mm (strongly positive); and one of six urine samples was positive for acid fast bacilli. Renal ultrasonography, chest X-ray, cervical, and thoracic spine X-rays were normal. The brain and cervical magnetic resonance imaging shown in [Figure 1] and [Figure 2], respectively were also normal. The cerebrospinal fluid (CSF) had slightly elevated protein (444 mg/L, normal 100-400/L), normal lymphocyte count (<5 cells), and glucose concentration (3.8 mmol/L, random blood glucose = 6.2 mmol/L). Hematologic indices were within normal limits (packed cell volume = 44.7%; haemoglobin = 14.3 g/dl; white blood cells = 8.0 × 10³/ul (neutrophils-63.3%, lymphocytes-18.6%, monocytes-12.4%, eosinophils-4.9%, basophils-0.8%); and platelet counts = 225 × 10³/ul). The liver enzymes (alanine transaminase: Aspartate transaminase ratio of 1.0), and serum urea (2.3 mmol/l) were normal. He was sero-negative to human immunodeficiency virus-I and II. There were no facilities for nerve conduction studies.
Figure 1: Sagittal View: Brain and cervical MRI showing no abnormality

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Figure 2: Coronal View: Brain MRI showing no abnormality

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Based on these results, a provisional diagnosis of TB-associated atypical polyradiculopathy was made, and he was commenced on oral daily doses of rifampicin 600 mg, pyrazinamide 1500 mg, ethambutol 800 mg, isoniazid 450 mg and pyridoxine 25 mg for 2 months. He was also commenced on physiotherapy, daily subcutaneous enoxaparin 40 mg, and oral prednisolone 15 mg. By the end of the intensive phase of anti-TB therapy, he was asymptomatic; fever remitted, muscle power in upper and lower limbs increased to 5/5 and 3/5 respectively. He was continued on oral daily rifampicin 600 mg, isoniazid 450 mg and pyridoxine 25 mg for 12 months. By the 10 th month of therapy, he was fully recovered and was discharged to follow-up.

  Discussion Top

TB affecting the central nervous system has been variously described in the forms of Pott's disease (TB of spinal vertebrae) and TB meningitis, but cases of TB associated peripheral neuropathy are not common. For instance, Hussein et al. in a study of 157 patients with neurological complications of TB at a teaching hospital in Sudan reported that 68% had meningitis, 30% had Pott's paraplegia and 2% had peripheral neuropathy. [1]

The few cases of TB-associated peripheral neuropathy reported in the literature have been postulated to result from direct Mycobacterial invasion of nerves, [4] immune-mediated vasculitic neuropathy, [5] antituberculous neurotoxicity, [6] and compressive neuropathy. [7],[8],[9] TB granulomas were responsible for 3 cases of the compressive neuropathies reported. These were compression of sural and median nerves leading to bilateral foot drop and carpal tunnel syndrome respectively, and compression of the cauda equine, which led to saddle anesthesia.

Although cases of chronic inflammatory demyelinating polyradiculopathy have been reported in patients with intestinal TB, [10] review of current literature has not revealed any report of polyradiculopathy in patients with renal or genitourinary TB. Acute flaccid quadriparesis, which is characterized by symmetric limb weakness and reduction or loss of tendon reflexes is usually caused by lesions of peripheral nerves (polyneuropathy) or the nerve roots (polyradiculopathy) in the absence of compressive myelopathy. [11]

The patient presented in this report had TB of the urinary tract complicated by acute flaccid quadriparesis and DSP. While TB was diagnosed by clinical and laboratory methods, the clinical diagnosis of acute flaccid quadriparesis and DSP was not supported by nerve conduction velocity (NCVs) and electromyography (EMG) studies as these electrophysiological tools were not available in our center. Although this was a limitation as NCVs and EMG studies are ancillary tools, which may reveal relevant findings consistent with demyelinating neuropathy and reduced motor recruitment proportional to the degree of weakness, the diagnosis of typical DSP is usually clinical. [11]

The mechanism of TB associated peripheral neurological diseases is largely unknown, but is thought to be immune-mediated or due to direct Mycobacterial invasion of nerves. The mild increase in the level of CSF protein which did not affect other parameters of the fluid may have resulted from inflammatory exudates around the meningeal coverings of peripheral nerve roots during either one or both of these two events. Additional supports were: The presence of constitutional symptoms (fever, night sweats, and malaise, and weight loss) of TB before the onset of the features of polyradiculopathy; and the improvement of neurological deficits following prednisolone and anti-tuberculous therapy.

In conclusion, this report with demonstrates rare neurological complication of urinary tract Tb and the efficacy of anti TB therapy in both conditions.

  References Top

1.Hussein A, Eltayeb AE, Sidig A, El Turabi H. MOEH gadour: The pattern of neurological manifestations of tuberculosis among adult Sudanese patients. Sudan J Med Sci 2008;3:221-6.  Back to cited text no. 1
2.Crofton J. Clinical tuberculosis. London: Macmillan Education; 2009.  Back to cited text no. 2
3.World Health Organization. Treatment of tuberculosis. Guidelines for National Programmes. Geneva: WHO; 2005.  Back to cited text no. 3
4.Jain SK, Paul-Satyaseela M, Lamichhane G, Kim KS, Bishai WR. Mycobacterium tuberculosis invasion and traversal across an in vitro human blood-brain barrier as a pathogenic mechanism for central nervous system tuberculosis. J Infect Dis 2006;193:1287-95.  Back to cited text no. 4
5.Stübgen JP. Myopathy and neuropathy due to tuberculous vasculitis. S Afr Med J 1992;81:436-7.  Back to cited text no. 5
6.van der Watt JJ, Harrison TB, Benatar M, Heckmann JM. Polyneuropathy, anti-tuberculosis treatment and the role of pyridoxine in the HIV/AIDS era: A systematic review. Int J Tuberc Lung Dis 2011;15:722-8.  Back to cited text no. 6
7.Kapoor SK, Garg V, Dhaon BK, Jindal M. Tuberculosis of the posterior vertebral elements: A rare cause of compression of the cauda equina. A case report. J Bone Joint Surg Am 2005;87:391-4.  Back to cited text no. 7
8.Orrell RW, King RH, Bowler JV, Ginsberg L. Peripheral nerve granuloma in a patient with tuberculosis. J Neurol Neurosurg Psychiatry 2002;73:769-71.  Back to cited text no. 8
9.Poulose SP, Sugath S, Gopalakrishnan KC. Tuberculosis affecting the median nerve. Kerala J Orthop 2011;24-5.  Back to cited text no. 9
10.Chong VH, Joseph TP, Telisinghe PU, Jalihal A. Chronic inflammatory demyelinating polyneuropathy associated with intestinal tuberculosis. J Microbiol Immunol Infect 2007;40:377-80.  Back to cited text no. 10
11.Dyck PJ. Detection, characterization, and staging of polyneuropathy: Assessed in diabetics. Muscle Nerve 1988;11:21-32.  Back to cited text no. 11


  [Figure 1], [Figure 2]


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